| 货号 | 10949S |
| 同种亚型 | Mouse IgG1 |
| 反应种属 | Human |
| 应用 | WB,IP,IHC,IF |
| 目标/特异性 | IRF-3 (D9J5Q) Mouse mAb recognizes endogenous levels of total IRF-3 protein. |
| 使用方法 | Western Blotting (1:1000) Immunoprecipitation (1:50) Immunohistochemistry (Paraffin) (1:400) Immunofluorescence (Immunocytochemistry) (1:400) |
| 供应商 | CST |
| 灵敏度 | Endogenous |
| 背景 | Interferon regulatory factors (IRFs) comprise a family of transcription factors that function within the Jak/Stat pathway to regulate interferon (IFN) and IFN-inducible gene expression in response to viral infection (1). IRFs play an important role in pathogen defense, autoimmunity, lymphocyte development, cell growth, and susceptibility to transformation. The IRF family includes nine members: IRF-1, IRF-2, IRF-9/ISGF3γ, IRF-3, IRF-4 (Pip/LSIRF/ICSAT), IRF-5, IRF-6, IRF-7, and IRF-8/ICSBP. All IRF proteins share homology in their amino-terminal DNA-binding domains. IRF family members regulate transcription through interactions with proteins that share similar DNA-binding motifs, such as IFN-stimulated response elements (ISRE), IFN consensus sequences (ICS), and IFN regulatory elements (IRF-E) (2). IRF-3 can inhibit cell growth and plays a critical role in controlling the expression of genes in the innate immune response (1-4). In unstimulated cells, IRF-3 is present in the cytoplasm. Viral infection results in phosphorylation of IRF-3 and leads to its translocation to the nucleus, where it activates promoters containing IRF-3-binding sites. Phosphorylation of IRF-3 occurs at a cluster of C-terminal Ser and Thr residues (between 385 and 405), leading to its association with the p300/CBP coactivator protein that promotes DNA binding and transcriptional activity (5). During infection, IRF-3 is likely activated through a pathway that includes activation of Toll-like receptors and a kinase complex that includes IKKε and TBK1 (6,7). IRF-3 is phosphorylated at Ser396 following viral infection, expression of viral nucleocapsid, and double-stranded RNA treatment. These events likely play a role in activation of IRF-3 (8). |
| 存放说明 | -20C |
| 计算分子量 | 50-55 |
| 参考文献 | 1 . Taniguchi, T. et al. (2001) Annu Rev Immunol 19, 623-55. 2 . Honda, K. and Taniguchi, T. (2006) Nat Rev Immunol 6, 644-58. 3 . Hiscott, J. et al. (1999) J Interferon Cytokine Res 19, 1-13. 4 . Kim, T.Y. et al. (2003) J Biol Chem 278, 15272-8. 5 . Yoneyama, M. et al. (2002) J Interferon Cytokine Res 22, 73-6. 6 . Fitzgerald, K.A. et al. (2003) Nat Immunol 4, 491-6. 7 . Kopp, E. and Medzhitov, R. (2003) Curr Opin Immunol 15, 396-401. 8 . Servant, M.J. et al. (2003) J Biol Chem 278, 9441-7. |
Confocal immunofluorescent analysis of HT-29 cells, untransfected (left) or transfected with Poly(I:C) (2.5 μg/mL, 6 hr; right), using IRF-3 (D9J5Q) Mouse mAb (green). Actin filaments were labeled with DyLight™ 554 Phalloidin #13054 (red). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye). Note the nuclear translocation of IRF-3 in a subset of cells (arrow). | |
Western blot analysis of extracts from various cell lines using IRF-3 (D9J5Q) Mouse mAb. | |
Immunoprecipitation of IRF-3 protein from U-937 cell extracts. Lane 1 is 10% input, Lane 2 is Mouse (G3A1) mAb IgG1 Isotype Control #5415, and lane 3 is IRF-3 (D9J5Q) Mouse mAb. Western blot analysis was performed using IRF-3 (D9J5Q) Mouse mAb. | |
Immunohistochemical analysis of paraffin-embedded human colon carcinoma using IRF-3 (D9J5Q) Mouse mAb. |
